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J. Biol. Chem., Vol. 275, Issue 48, 37915-37921, December 1, 2000
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From the Institute of Genetics, University of Cologne,
Weyertal 121, D-50931 Koeln, Germany
The chloramphenicol acetyltransferase gene under
the control of the late E2A promoter of adenovirus type 2 (Ad2) was
introduced as transgene into the B6D2F1 mouse strain with mixed genetic
background and became extensively de novo methylated. The
methylation of this pAd2E2AL-CAT (7-1A) transgene
was regulated in a strain-specific manner apparently depending on the
site of integration. Transmission of the 7-1A transgene
into an inbred DBA/2, 129/sv, or FVB/N genetic background led to a
significant loss of methylation in the transgene, whereas C57BL/6,
CB20, and Balb/c backgrounds favored the de novo methylation in very specific patterns. The newly established patterns of de novo methylation were transmitted to the offspring
and remained stable for many generations, regardless of the
heterozygosity of strain-specific DNA sequences present in these mouse
strains. Segregation analyses showed a non-mendelian transmission of
methylation phenotypes and suggested the involvement of dominant
modifiers of methylation. The genotype-specific modifications of the
transgene were followed for 11 backcross generations. These
observations reflect an evolutionarily conserved mechanism directed
against foreign, e.g. viral or bacterial, DNA at least in
the chromosomal location of the 7-1A transgene. In seven
additional mouse lines carrying the same transgene in different
chromosomal locations, strain-specific alterations of methylation
patterns were not observed.
Epigenetic and Genotype-specific Effects on the Stability of
de Novo Imposed Methylation Patterns in Transgenic
Mice*
,
*
This work was supported in part by Deutsche
Forschungsgemeinschaft Grant SFB274-A1, by the Center for Molecular
Medicine Koeln, TV13, and EU Contract BMH4-CT96-0050.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Present address: Qiagen GmbH, Max-Volmer Strasse 4, D-40724
Hilden, Germany.
§
Present address: 1135 Stanyan St., San Francisco, CA 94117. Supported by a fellowship of the Alexander von Humboldt Stiftung.
¶
To whom correspondence should be addressed: Institute of
Genetics, University of Cologne, Weyertal 121, D-50931 Koeln, Germany. Tel: 49-221-470-2386; Fax: 49-221-470-5163; E-mail:
doerfler@scan. genetik.uni-koeln.de.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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